| Name | calmodulin |
|---|---|
| Synonyms | CALM; CAM; CALM 1; CALM 2; CALM 3; CALM1; CALM2; CALM3… |
| Name | diphenylamine |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 9108631 | Iwase N, Sasaki T, Shimura S, Yamamoto M, Suzuki S, Shirato K: ATP-induced Cl- secretion with suppressed Na+ absorption in rabbit tracheal epithelium. Respir Physiol. 1997 Feb;107(2):173-80. The initial increase by ATP (10 (-4) M) was significantly inhibited by a Cl (-) -channel inhibitor diphenylamine-2-carboxylate (DPC, 5 x 10 (-4) M) and Cl (-) -substitution with in the bath solution, while a cystic fibrosis transmembrane regulator (CFTR) Cl (-) -channel inhibitor glibenclamide (10 (-4) M), a Na (+)-channel inhibitor amiloride (10 (-4) M) and a K (+) -channel inhibitor quinidine (10 (-4) M) all failed to alter it. A calmodulin antagonist W-7 reduced the SCC baseline and abolished SCC increase by ATP. |
1(0,0,0,1) | Details |
| 9618558 | Mitchell CH, Carre DA, McGlinn AM, Stone RA, Civan MM: A release mechanism for stored ATP in ocular ciliary epithelial cells. . Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):7174-8. ATP release also was triggered by ionomycin through a different NPPB-insensitive mechanism, inhibitable by the /calmodulin-activated kinase II inhibitor KN-62. In contrast, the P-glycoprotein inhibitors tamoxifen and and the cystic fibrosis transmembrane conductance regulator (CFTR) blockers glybenclamide and diphenylamine-2-carboxylate did not affect ATP release from either cell type. |
1(0,0,0,1) | Details |
| 8568845 | Ikeda K, Wu D, Takasaka T: Cellular mechanisms in activation of Na-K-Cl cotransport in nasal gland acinar cells of guinea pigs. J Membr Biol. 1995 Aug;146(3):307-14. Moreover, both a calmodulin antagonist trifluoperazine and a myosin light chain kinase inhibitor ML-7 reduced the -induced response in [Na+] i. However, the following treatment did not affect the basal [Na+] i nor the -induced increase in [Na+] i: (i) addition of dibutyryl cAMP, 8-Br- or phorbol 12- 13- (ii) pretreatment of protein kinase inhibitors, H-89, H-8, H-7 or chelerythrine, (iii) prevention of cytosolic Cl- efflux by the addition of diphenylamine-2-carboxylic acid or, (iv) prevention of cytosolic K+ efflux by the addition of charybdotoxin.(ABSTRACT TRUNCATED AT 250 WORDS) |
1(0,0,0,1) | Details |
| 7202016 | Rochette-Egly C, Boschetti E, Basset P, Egly JM: Interactions between calmodulin and immobilized phenothiazines. J Chromatogr. 1982 Jun 4;241(2):333-44. However, the Ca2+-dependent binding of calmodulin was less specific with phenothiazine structural analogues (neutral Red, diphenylamine) and was suppressed with other phenothiazine derivatives (thionine, Azure C, Toluidine Blue) or analogues (Brilliant Cresyl Blue). |
37(0,1,1,7) | Details |
| 6087521 | Walter RD, Albiez EJ: Interaction of amoscanate with the -phosphodiesterases from Schistosoma mansoni, Onchocerca volvulus and bovine heart. Tropenmed Parasitol. 1984 Jun;35(2):78-80. The anthelmintic compounds amoscanate (4-isothiocyanato-4'-nitrodiphenylamine) and its derivatives CGP 6140 and CGP 8045 are potent inhibitors of the activities of -phosphodiesterases from schistosomal and filarial worms as well as from both the calmodulin-dependent and the -independent enzyme of bovine heart. |
1(0,0,0,1) | Details |
| 2560805 | Yoshida S, Plant S, Taylor PL, Eidne KA: channels mediate the response to gonadotropin-releasing hormone (GnRH) in Xenopus oocytes injected with rat anterior pituitary mRNA. Mol Endocrinol. 1989 Dec;3(12):1953-60. This GnRH response was blocked by the Cl- channel blockers 9-AC (9-anthracene carboxylic acid; 1 mM), 4,4'-diisothiocyanastilbene-2,2'-disulfonic acid (0.1 mM), and diphenylamine-2-carboxylic acid (0.1 mM). Ca2+ also plays a role, as the GnRH-induced response was reversibly suppressed by a calmodulin inhibitor, chlordiazepoxide (0.2 microM), and by a blocker of intracellular Ca2+ release, TMB-8 (8-(N.N-diethylamino) octyl-3,4,5-trimethoxybenzoate; 0.1-0.2 mM). |
1(0,0,0,1) | Details |
| 8568854 | Chan HC, Zhou WL, Wong PY: Extracellular ATP activates both Ca (2+)- and cAMP-dependent Cl- conductances in rat epididymal cells. J Membr Biol. 1995 Sep;147(2):185-93. When applied to the later phase of the ATP-activated whole-cell current, the disulfonic acid stilbene DIDS (200 microM) could only inhibit 64% of the current while diphenylamine-dicarboxylic acid (DPC, 1 mM) completely inhibited it. Increased pipette EGTA (10 mM) or treatment of the cells with trifluoperazine (40 microM), an inhibitor of calmodulin, suppressed both types of ATP-induced Cl- currents. |
1(0,0,0,1) | Details |
| 12974684 | Ohshima K, Shiba Y, Hirono C, Sugita M, Iwasa Y, Shintani H: Luminal space enlargement by carbachol in rat parotid intralobular ducts. Eur J Oral Sci. 2003 Oct;111(5):405-9. Diphenylamine-2-carboxylate (DPC), but not cytochalasin D, calmodulin inhibitor or synthase inhibitor profoundly suppressed CCh-induced changes. |
0(0,0,0,0) | Details |